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Beschreibung

G protein-activated inward rectifier potassium channel 4 (UniProt P48544, also known as Cardiac inward rectifier, CIR, Heart KATP channel, Inward rectifier K(+) channel Kir3.4, GIRK-4, IRK-4, KATP-1, Potassium channel, inwardly rectifying subfamily J member 5) is encoded by the KCNJ5 (also known as GIRK4, LQT13) gene (Gene ID 3762) in human. Inward rectifier K+ channels (Kirs) modulate cell membrane potential and are classified as K+ transport channels (Kir1.x, Kir4.x, Kir5.x, Kir7.x), classic Kir (Kir2.x), G-protein-gated Kirs (Kir2.x and Kir3.x), and ATP-sensitive Kirs (Kir6.x). Kirs mediate diverse physiological functions of both excitable and nonexcitable epithelial cells, such as cell adhesion-migration, volume regulation, apoptosis, and proliferation. While a large fraction of Kir3.4 (GIRK4, KCNJ5) subunits is processed to the cell membrane to form homomultimers, Kir3.4 subunits also assemble into heteromeric channels with Kir3.1 (GIRK1, KCNJ3) subunits in atrial myocytes or Kir3.2 (GIRK2, KCNJ6) in the cerebellum. Upon agonist activation of appropriate GPCRs, heteroterameric Kir3.4 channels are opened via interaction with subunits of the pertussis toxin-sensitive class (Gi/o) G-proteins, resulting in membrane hyperpolarization and/or reduced excitability. Whereas homotetrameric Kir3.4 channels can be activated by high intracellular Na+ independent of G-protein. Human Kir3.4 is a 419-amino acid multi-pass membrane (a.a. 87-111, 136-147, 164-185) protein that contains two small extraceullar regions (a.a. 112-135 and 155-163) and a pore-forming domain (a.a. 148-154), having both its N- and C-terminal ends exposed intracellularly (a.a. 1-86 and a.a. 186-419).

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